fldA is an essential gene required in the 2-C-methyl-D-erythritol 4-phosphate pathway for isoprenoid biosynthesis
fldA is an essential gene required in the 2-C-methyl-D-erythritol 4-phosphate pathway for isoprenoid biosynthesis
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DOI：
10.1016/j.febslet.2005.05.047
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发表时间：
2005-07-04
期刊：
影响因子：
3.5
通讯作者：
Morita, CT
中科院分区：
文献类型：
--
作者：
Puan, KJ;Wang, H;Morita, CT
虽然黄素氧还蛋白I是大肠杆菌生长所必需的，但黄素氧还蛋白I是必需的确切途径尚未确定。我们在大肠杆菌中对flavodoxin I基因fldA进行了转座子诱变。大肠杆菌菌株，其表达甲羟戊酸途径酶并且在MEP途径的lytB基因中具有点突变，导致（E）-4-羟基-3-甲基丁基-2-烯基焦磷酸（HMBPP）的积累。fldA的破坏废除了甲羟戊酸盐非依赖性生长，并显着降低HMBPP水平。fldA（-）突变体与甲羟戊酸一起生长，表明黄素氧还蛋白I在有氧条件下的重要作用是在MEP途径中。通过fldA互补恢复生长。由于GcpE（合成HMBPP）和LytB是铁硫酶，需要一个还原系统的活动，我们建议，黄素氧还蛋白是必不可少的GcpE和可能的LytB的活动。因此，flavodoxin I在E.大肠杆菌是类异戊二烯生物合成的MEP途径。(c)2005年欧洲生物化学学会联合会。Elsevier B. V.出版，保留所有权利。
Although flavodoxin I is indispensable for Escherichia coli growth, the exact pathway(s) where flavodoxin I is essential has not been identified. We performed transposon mutagenesis of the flavodoxin I gene, fldA, in an E. coli strain that expressed mevalonate pathway enzymes and that had a point mutation in the lytB gene of the MEP pathway resulting in the accumulation of (E)-4-hydroxy-3-methylbutyl-2-enyl pyrophosphate (HMBPP). Disruption of fldA abrogated mevalonate-independent growth and dramatically decreased HMBPP levels. The fldA(-) mutant grew with mevalonate indicating that the essential role of flavodoxin I under aerobic conditions is in the MEP pathway. Growth was restored by fldA complementation. Since GcpE (which synthesizes HMBPP) and LytB are iron-sulfur enzymes that require a reducing system for their activity, we propose that flavodoxin is essential for GcpE and possibly LytB activity. Thus, the essential role for flavodoxin I in E. coli is in the MEP pathway for isoprenoid biosynthesis. (c) 2005 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.